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1.
Distribution of Ankyrin Isoforms and Their Proteolysis After Ischemia and Reperfusion in Rat Brain 总被引:1,自引:0,他引:1
Kazuki Harada Shiro Fukuda †Manabu Kunimoto Ken-ichi Yoshida 《Journal of neurochemistry》1997,69(1):371-376
Abstract: The distribution of brain-type ankyrin (ankyrinB , 212 kDa) and erythrocyte-type ankyrin (ankyrinR , 239 kDa) was investigated in the subcellular fractions of rat forebrain (P1, 1,000 g pellet; P2, 15,000 g pellet; P3, 100,000 g pellet; S, 100,000 g supernatant) by immunoblotting using specific antibodies. The P2 fraction contained ∼40% of the 212- and 163-kDa isoforms of ankyrinB and the 239-kDa isoform of ankyrinR . Further subfractionation of the P2 by Percoll gradient centrifugation followed by separation of myelin showed association of the three ankyrin isoforms with the synaptosome-rich fraction but not with the myelin-rich fraction. The plasma membrane-rich P3 fraction contained a concentration of ankyrin isoforms similar to that in the P2 fraction. In vitro proteolysis of ankyrin in the P2 fraction with calpain showed that the 212-kDa ankyrinB was more susceptible to calpain than was ankyrinR . In the two-vessel occlusion model, ischemia for 30 min generated the 160-kDa fragment of ankyrinR , and reperfusion for 60 min after 30 min of ischemia remarkably increased the 160-kDa fragment. The reperfusion also significantly decreased the 212-kDa isoform of ankyrinB . Both ischemia-reperfusion and in vitro proteolysis with calpain generated the 160-kDa fragment of ankyrinR , suggesting the involvement of calpain. 相似文献
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Taiichiro Okajima Toshiharu Motomatsu Ken-ichi Kato Hiroshi Ibayashi 《Life sciences》1980,26(9):699-705
Intraventicular injection of beta-endorphin (beta LPH61?91) in urethane anesthetized male rats led to a dose dependent increase of plasma prolactin levels. Intravenous injection of apomorphine completely abolished the stimulatory effect of beta-endorphin. Animals treated with 6-hydroxydopamine (6-OHDA) and 6-OHDA plus desmethylimipramine showed inhibition of beta-endorphin induced prolactin release. These results suggest that beta-endorphin presynaptically inhibits the activity of dopaminergic neurones, leading to the stimulation of plasma prolactin levels. 相似文献
3.
M Tachibana H Morioka M Machino F Mizukoshi O Mizukoshi T Yoshioka 《Histochemistry》1985,82(2):197-199
Triphosphoinositide (TPI), an aminoglycoside receptor and a possible regulator of cationic permeation through its ability to bind with Ca++, was localized by the protein-A gold technique in vestibular sensory epithelia using an antibody highly specific to TPI. TPI was detected on the stereocilia, kinocilia, and cuticular plate of hair cells, and in the reticular membrane of supporting cells. The cilia of hair cells are damaged by aminoglycosides at a relatively early stage of toxicity. Ca++-regulated bioactivity in this area is probably involved. 相似文献
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In several vascular inflammatory reactions (i.e. immunity and thrombosis) inflammatory mediators lead to the activation of vascular endothelial cells (EC). To date, a number
of functional molecules induced on the surface of activated-EC have been identified. We report here that Globotetraosylceramide
(Gb4), a glycosphingolipid expressed in EC, is a novel inducible molecule on EC activated by TNF-α. The cell surface expression
of Gb4 is increased in a time-dependent manner under TNF-α stimulation, which shows distinct expression kinetics of major
proteins induced by TNF-α on EC. MALDI-TOF-MS analysis revealed that the enhanced Gb4 predominantly contains C24:0 fatty acid
in the ceramide moiety. Isolated caveolae/lipid raft-enriched detergent insoluble membrane domains in activated-EC predominantly
contain this molecular species of Gb4. Gb4 containing C16:0 fatty acid in the ceramide moiety, which is known to constitute
the major species of Gb4 in plasma, is also found as a major molecular species in EC. These observations indicate that Gb4,
especially with very long fatty acid, is enhanced in EC during its inflammatory reaction, and suggest the potential utility
of Gb4 as a biomarker for monitoring inflammation status of EC involving its related diseases. 相似文献
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